Psychiatr News November 17, 2006
Volume 41, Number 22, page 25
© 2006 American Psychiatric Association
Zinc May Play Major Role In Mechanism of Fear
Joan Arehart-Treichel
New insights into the molecular mechanisms governing fear—for
example, that the metal zinc is involved—may lead to a new
classification of anxiety states and new types of antianxiety drugs.
Although fear is known to arise from the amygdala—that almond-shaped
labyrinth located in front of the hippocampus—the molecular mechanisms
of fear production have remained elusive.
Then, a few months ago, Gleb Shumyatsky, Ph.D., an assistant professor of
genetics at Rutgers University; Nobel Prize–winning psychiatrist Eric
Kandel, M.D., of Columbia University, and colleagues reported that a protein
called stathmin, made in the amygdala, appears to be crucial for both the
expression of innate fear and the formation of memory for learned fear
(Psychiatric News, February 3).
Now more insights into the molecular mechanics of fear production appear to
have been obtained by Shumyatsky, Kandel, and their group, and the metal zinc
seems to be a crucial player. Results were published in the September 27
online early edition of the Proceedings of the National Academy of
Sciences.
First the scientists found that zinc is plentiful in sections of the rat
amygdala as well as in the rat auditory cortex, which sends auditory
information to the amygdala during fear learning. Then they discovered that
those nerves in the rat amygdala that use the neurotransmitter glutamate
release zinc as well as glutamate when communicating with each other, and that
release boosts electrical transmission between the nerves.
Thus zinc may well contribute to the learning of fear, the researchers
concluded. Or as the lead researcher, Vadim Bolshakov, Ph.D., director of the
Cellular Neurobiology Laboratory at McLean Hospital, put it in an accompanying
press release: "Our results provide the first direct evidence that zinc
released during the communication between neurons has an impact on
neurotransmission in the amygdala, thus potentially contributing to fear
learning."
The findings may also lead to a new classification of anxiety disorders,
Shumyatsky told Psychiatric News. "Our new study, along with
our earlier work... demonstrates that the neuroanatomic circuits of fear and
fear behaviors have their own molecular substrates. This, in turn, suggests
that anxiety disorders are not of one common molecular origin, but instead
have their specific molecular signatures..., and perhaps in the future will
allow for a new type of classification of anxiety states according not only to
their behavioral phenotypes, but also with regard to their anatomic and
molecular characteristics."
And the results might even lead to new antianxiety drugs, Shumyatsky
speculated. "In our study, a gene encoding [the zinc transporter, which
is a specific marker for zinc-containing nerves, was] expressed in the
cortico-amygdala pathway, but not in the thalamo-amygdala pathway. These two
parallel neural pathways are important in relaying fearful stimulus
information... to the amygdala. Which of these two pathways is more important,
or whether they are equally important, for fear behavior is not clear yet.
However, their differences in zinc requirement suggest [that we might be able
to design drugs] to target one type of fear processing versus
another."
The study was funded by the National Institutes of Health, the Esther A.
and Joseph Klingenstein Fund, the National Alliance for Research on
Schizophrenia and Depression, the New Jersey Governor's council on Autism, and
the Charles and Johanna Busch Memorial Fund.
An abstract of "Synaptically Released Zinc Gates Long-Term
Potentiation in Fear Conditioning Pathways" is posted at
<www.pnas.org/cgi/content/abstract/0607131103v1>.
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